Key result
LVNC linked to ~1.7 g/m2 higher myocardial mass difference vs. controls on CMR.
Why the study?
Current CMR criteria for LVNC rely on static morphologic thresholds and may not adequately reflect dynamic myocardial adaptation.
Does absolute myocardial mass difference (AD) measured by cardiovascular magnetic resonance help distinguish morphologically defined left ventricular non-compaction from normal myocardium and correlate with structural-functional remodeling?
Case-Control (n=165)
Does absolute myocardial mass difference (AD) measured by cardiovascular magnetic resonance help distinguish morphologically defined left ventricular non-compaction from normal myocardium and correlate with structural-functional remodeling?
Standardized Mean Difference: 0.81
Absolute Event Rate: 3.71% vs 2.03%
p-value: p=<0.001
Absolute myocardial mass difference (AD) derived from CMR is increased in morphologically defined left ventricular non-compaction and may serve as a marker of dynamic structural-functional remodeling.
Background Left ventricular non-compaction (LVNC) is increasingly recognized as a morphological phenotype rather than a distinct cardiomyopathy. Current cardiovascular magnetic resonance (CMR) criteria rely predominantly on static morphologic thresholds and may not adequately reflect dynamic myocardial adaptation. Purpose To investigate whether absolute myocardial mass difference (AD) represents a marker of structural–functional remodeling and to assess its relationship with hemodynamic and flow-related parameters in morphologically defined LVNC. Material and Methods In this retrospective study, 99 patients fulfilling Petersen and Grothoff CMR criteria for LVNC and 66 frequency-matched controls underwent multiparametric 1.5-T CMR. Volumetric indices, left atrial volume, cine-derived functional parameters, and aortic phase-contrast MRI flow timing indices, including time-to-peak velocity (TPV), ejection time (ET), and TPV/ET ratio, were analyzed. AD was defined as the indexed difference between end-diastolic myocardial mass and cycle-averaged myocardial mass. Between-group comparisons, effect size analysis, correlation testing, and ROC analysis were performed. Results AD was significantly higher in LVNC patients than in controls (3.71 ± 2.43 vs. 2.03 ± 1.49 g/m 2 ; P < 0.001) and demonstrated a large effect size (Cohen's d = 0.81). LVNC patients exhibited increased end-diastolic and end-systolic volume indices (both P < 0.001), preserved cardiac index, and altered systolic flow timing characteristics. AD correlated positively with left atrial volume ( r = 0.39; P < 0.001) and cardiac index ( r = 0.27; P = 0.007), whereas no significant association was observed with TPV/ET. ROC analysis demonstrated modest discriminatory performance (AUC = 0.71). Conclusion In morphologically defined LVNC, AD is increased and associated with atrial remodeling and preserved hemodynamic adaptation. These findings suggest that AD may represent a marker of dynamic structural–functional remodeling rather than static trabecular excess. Incorporation of AD into multiparametric CMR assessment may improve phenotypic characterization and help distinguish compensated hypertrabecularization from clinically relevant myocardial disease.
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Bulut et al. (2026) conducted a case-control in Left ventricular non-compaction (n=165). Morphologically defined left ventricular non-compaction vs. Frequency-matched controls was evaluated on Absolute myocardial mass difference (AD) (Cohen's d 0.81, p=<0.001). Morphologically defined LVNC was associated with a significantly higher absolute myocardial mass difference compared to controls (3.71 vs. 2.03 g/m2; P<0.001, Cohen's d=0.81).
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